Molecular Human Reproduction, Vol. 6, No. 11, 1019-1025,
November 2000
© 2000 European Society of Human Reproduction and Embryology
Pregnancy |
p57Kip2 regulates the proper development of labyrinthine and spongiotrophoblasts
1 Molecular Oncology Group, Nippon Roche Research Center 200, Kajiwara, Kamakura, Kanagawa 247-8530, and 2 Department of Obstetrics and Gynecology, Hamamatsu University School of Medicine 3600, Handa-cho, Hamamatsu, Shizuoka 431-3192, Japan
Abstract
The cyclin-dependent kinase (cdk) inhibitor, p57 Kip2 is a tumour suppressor candidate and a paternally-imprinted gene. In humans, the p57Kip2 gene is located on chromosome 11p15.5, a region implicated in both sporadic cancers and Beckwith–Wiedemann syndrome. From analysis of p57Kip2-deficient mice, we demonstrate the relationship between trophoblastic abnormalities and p57Kip2. Both p57Kip2 null (–/–) embryos and heterozygous embryos with a maternally-derived mutated allele (+*/–) displayed placentomegaly, as well as dysplasia of labyrinthine and spongiotrophoblasts. The number of labyrinthine trophoblasts of homozygous embryos was twice that in wild-type embryos. When we measured kinase activities of cdk in total placenta lysates by the immuno complex kinase assay, there were no differences among the genotypes. These results show that p57Kip2 may function in the proper development of labyrinthine and spongiotrophoblasts by pathways that are not involved with regulation of cdk activities. It is, therefore, suggested that p57Kip2 protein might have an unknown role.
Beckwith-Wiedemann syndrome/choriocarcinoma/cyclin-dependent kinase inhibitor/imprinting//tumour suppressor gene
Notes
3 To whom correspondence should be addressed at the current address: Department of Physiological Chemistry, School of Pharmaceutical Sciences, Showa University 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan. E-mail: takahask{at}pharm.showa-u.ac.jp
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